Summary of Study ST001709

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001094. The data can be accessed directly via it's Project DOI: 10.21228/M89394 This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST001709
Study TitleSARS-CoV-2 infection rewires host cell metabolism and is potentially susceptible to mTORC1 inhibition
Study SummaryViruses hijack host cell metabolism to acquire the building blocks required for viral replication. Understanding how SARS-CoV-2 alters host cell metabolism could lead to potential treatments for COVID-19, the disease caused by SARS-CoV-2 infection. Here we profile metabolic changes conferred by SARS-CoV-2 infection in kidney epithelial cells and lung air-liquid interface cultures and show that SARS-CoV-2 infection increases glucose carbon entry into the TCA cycle via increased pyruvate carboxylase expression. SARS-CoV-2 also reduces host cell oxidative glutamine metabolism while maintaining reductive carboxylation. Consistent with these changes in host cell metabolism, we show that SARS-CoV-2 increases activity of mTORC1, a master regulator of anabolic metabolism, in cell lines and patient lung stem cell-derived airway epithelial cells. We also show evidence of mTORC1 activation in COVID-19 patient lung tissue. Notably, mTORC1 inhibitors reduce viral replication in kidney epithelial cells and patient-derived lung stem cell cultures. This suggests that targeting mTORC1 could be a useful antiviral strategy for SARS-CoV-2 and treatment strategy for COVID-19 patients, although further studies are required to determine the mechanism of inhibition and potential efficacy in patients.
Institute
University of California, Los Angeles
DepartmentBiomedical Sciences
LaboratoryHeather Christofk
Last NameMatulionis
First NameNedas
Address615 Charles E Young Dr S, BSRB 354-05
Emailnmatulionis@mednet.ucla.edu
Phone310-206-0163
Submit Date2021-02-19
Raw Data AvailableYes
Raw Data File Type(s)mzML
Analysis Type DetailLC-MS
Release Date2021-02-24
Release Version1
Nedas Matulionis Nedas Matulionis
https://dx.doi.org/10.21228/M89394
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR001094
Project DOI:doi: 10.21228/M89394
Project Title:SARS-CoV-2 infection rewires host cell metabolism and is potentially susceptible to mTORC1 inhibition
Project Summary:Viruses hijack host cell metabolism to acquire the building blocks required for viral replication. Understanding how SARS-CoV-2 alters host cell metabolism could lead to potential treatments for COVID-19, the disease caused by SARS-CoV-2 infection. Here we profile metabolic changes conferred by SARS-CoV-2 infection in kidney epithelial cells and lung air-liquid interface cultures and show that SARS-CoV-2 infection increases glucose carbon entry into the TCA cycle via increased pyruvate carboxylase expression. SARS-CoV-2 also reduces host cell oxidative glutamine metabolism while maintaining reductive carboxylation. Consistent with these changes in host cell metabolism, we show that SARS-CoV-2 increases activity of mTORC1, a master regulator of anabolic metabolism, in cell lines and patient lung stem cell-derived airway epithelial cells. We also show evidence of mTORC1 activation in COVID-19 patient lung tissue. Notably, mTORC1 inhibitors reduce viral replication in kidney epithelial cells and patient-derived lung stem cell cultures. This suggests that targeting mTORC1 could be a useful antiviral strategy for SARS-CoV-2 and treatment strategy for COVID-19 patients, although further studies are required to determine the mechanism of inhibition and potential efficacy in patients.
Institute:University of California, Los Angeles
Department:Biomedical Sciences
Laboratory:Heather Christofk
Last Name:Matulionis
First Name:Nedas
Address:615 Charles E Young Drive South Los Angeles, CA 90095
Email:nmatulionis@mednet.ucla.edu
Phone:310-206-0163
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